The Origins of Ventricular Arrhythmias

Using the ECG as a Key Tool for Localization

Frank M. Bogun, MD

• Publisher: Cardiotext Publishing
• Year: 2018
• Print ISBN: 9781942909224
• eBook ISBN: 9781942909279
• Edition: 1
• Topic: Medicine
• Subtopic: Cardiology

This illustrated text teaches electrophysiology and cardiology fellows-in-training the concept of connecting ventricular arrhythmias' QRS morphology with the arrhythmia site of origin. Thirty case studies, including multimodality imaging and anatomy data, illustrate the precise locations of the sites of origin of different ventricular arrhythmias. Mapping approaches are discussed, with an emphasis on how the 12-lead ECG helps to identify critical sites of the arrhythmias.

Illustrated with 106 figures that include 12-lead ECGs, intracardiac ECG tracings, and electroanatomical maps that are complemented by reconstructed intracardiac echo images.

CASE

1

CLINICAL HISTORY

A 47-year-old man presented with recurrent palpitations and decreased left ventricular ejection fraction of 45%. He had frequent premature ventricular complexes (PVC) with a PVC burden of 24% based on a Holter monitor. He had no delayed enhancement on cardiac MRI and no ischemia on stress testing. Beta-blocker therapy failed to reduce his palpitations. The patient was agreeable to an ablation procedure.

Question

Figure 1.1 shows the 12-lead ECG of the predominant PVC. Where does the PVC originate?

Figure 1.1 A 12-lead ECG showing a bigeminal rhythm with right bundle branch block inferior axis (RBBBIA) morphology.

Answer

The origin of the PVC was the lateral mitral valve annulus (MVA). This needs to be distinguished from an origin at the anterolateral (AL) papillary muscle (PAP). In fact, the pace map from the PAP was very similar to the pace map from the site of origin (SOO) at the MVA. The R/S transition here is lead V₆. Usually for PAP arrhythmias, the transition is earlier, at V₄ or sometimes V₃, but it can also be at V₅ or V₆.¹ Tada et al.² describe s and S waves in leads V₆, but at the time of their publication in 2005, PAP arrhythmias had not yet been described as a distinct entity, and some of their patients might have had PAP arrhythmias. If the transition is at lead V₅/V₆ in patients with PAP arrhythmias, the PAP may insert closer to the MVA. It is even possible that the PAP inserts directly into the MVA (this is also called mitral arcade or hammock valve). This results in positive concordance without transition. For arrhythmias originating further away from the anterior MVA, i.e., the lateral or posterior MVA, there is often no positive concordance as one might expect and the transition, despite an annular origin, may be at V₄–V₆. Therefore, PAP origins will need to be kept in the differential for this case as well. At the SOO, the local activation time was –25 ms (Figure 1.2) with a matching pace map (Figure 1.3) when pacing was performed at this site (Figure 1.4). A matching pace map at a site of early activation indicates that the catheter is located at or close to the SOO of the ventricular arrhythmia. If the pace map does not match at a site with early activation, the origin may be located deeper in the tissue.

Figure 1.2 Intracardiac tracings from the ablation catheter (Abl) at the site of origin in the anterolateral mitral valve annulus. The local activation time is –25 ms.

Figure 1.3 Left panel: A 12-lead ECG of the targeted PVC. Right panel: Pace mapping at the site of origin indicating a match of the pace map with the targeted PVC morphology.

Figure 1.4 A posterior view of the 3D reconstruction of the intracardiac echocardiographic contours of left and right ventricles (RV and LV). The catheter is shown with the tip at the site of origin at the anterolateral mitral valve annulus (white arrow). Red tags indicate the sites where radiofrequency energy was delivered. The papillary muscles are also displayed in green with the anterolateral papillary muscle (AL PAP) located at 11 o’clock and the posteromedial papillary muscle (PM PAP), located at a 6 o’clock position of the mitral annulus (MA).

REFERENCES

1.Good E, Desjardins B, Jongnarangsin K, et al. Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: A comparison with fascicular arrhythmias. Heart Rhythm. 2008;5:1530–1537.

2.Tada H, Ito S, Naito S, et al. Idiopathic ventricular arrhythmia arising from the mitral annulus: A distinct subgroup of idiopathic ventricular arrhythmias. J Am Coll Cardiol. 2005;45:877–886.

CASE

2

CLINICAL HISTORY

A 58-year-old man presented with nonischemic cardiomyopathy and an ejection fraction of 32%. Based on imaging, there was a lateral left wall scar noted on the MRI. He had frequent PVCs, with a PVC burden of 35%, and presented for PVC ablation after an attempted ablation procedure elsewhere failed. A total of seven different PVCs were present; attached is one of his clinical PVCs.

Question

Where does the PVC shown in Figure 2.1 originate from?

Figure 2.1 A 12-lead ECG of the patient’s PVC.

Answer

The PVC originates from the posteroseptal tricuspid valve area close to the bundle of His. The features suggestive of an origin close to the His bundle are: Q wave in lead V₁, R-wave amplitude in lead I > R-wave amplitude of the inferior leads, initial R wave in lead aVL. This constellation should prompt the operator to start the mapping procedure in the tricuspid valve area, close to the His area.¹ The ECG is not precise enough to indicate how close the SOO is located to the His. In this case, the origin was about 1 cm distal to the maximal His bundle deflection on the inferior wall and could be ablated from there at a site with an activation time of –27 ms (Figure 2.2) and a matching pace map (Figure 2.3). The R wave in lead I is larger than for right ventricular outflow tract (RVOT) arrhythmias because the parahisian/tricuspid valve area is located more to the right side of the RVOT (Figure 2.4). This is also the reason for a positive initial deflection in aVL. Often the R-wave transition in the precordial leads is much earlier at V_2...

Table of contents

• Cover
• Title Page
• Copyright
• Dedication
• FOREWORD
• PREFACE
• ABBREVIATIONS
• CASE 1
• CASE 2
• CASE 3
• CASE 4
• CASE 5
• CASE 6
• CASE 7
• CASE 8
• CASE 9
• CASE 10
• CASE 11
• CASE 12
• CASE 13
• CASE 14
• CASE 15
• CASE 16
• CASE 17
• CASE 18
• CASE 19
• CASE 20
• CASE 21
• CASE 22
• CASE 23
• CASE 24
• CASE 25
• CASE 26
• CASE 27
• CASE 28
• CASE 29
• CASE 30
• APPENDIX